scholarly journals Angiotensinergic stimulation of vascular endothelium in mice causes hypotension, bradycardia, and attenuated angiotensin response

2006 ◽  
Vol 103 (50) ◽  
pp. 19087-19092 ◽  
Author(s):  
R. Ramchandran ◽  
T. Takezako ◽  
Y. Saad ◽  
L. Stull ◽  
B. Fink ◽  
...  
Keyword(s):  
Vascular Endothelium ◽  
Stimulation Of

ATP and acetylcholine interact to modulate vascular tone and α1-adrenergic vasoconstriction in humans

2021 ◽  
Author(s):  
Janée D. Terwoord ◽  
Matthew L. Racine ◽  
Christopher M. Hearon ◽  
Gary J. Luckasen ◽  
Frank A. Dinenno
Keyword(s):  
Blood Flow ◽  
Vascular Endothelium ◽  
Vascular Tone ◽  
Complex Signal ◽  
Similar Response ◽  
Vascular Conductance ◽  
Arterial Infusion ◽  
Vasoconstrictor Response ◽  
Forearm Vascular Conductance ◽  
Stimulation Of

The vascular endothelium senses and integrates numerous inputs to regulate vascular tone. Recent evidence reveals complex signal processing within the endothelium, yet little is known about how endothelium-dependent stimuli interact to regulate blood flow. We tested the hypothesis that combined stimulation of the endothelium with adenosine triphosphate (ATP) and acetylcholine (ACh) elicits greater vasodilation and attenuates α1‑adrenergic vasoconstriction compared to combination of ATP or ACh with the endothelium-independent dilator sodium nitroprusside (SNP). We assessed forearm vascular conductance (FVC) in young adults (6F, 7M) during local intra-arterial infusion of ATP, ACh, or SNP alone and in the following combinations: ATP+ACh, SNP+ACh, and ATP+SNP wherein the second dilator was co-infused after attaining steady-state with the first dilator. By design, each dilator evoked a similar response when infused separately (ΔFVC, ATP: 48±4; ACh: 57±6; SNP: 53±6 ml·min-1·100 mmHg-1; P≥0.62). Combined infusion of the endothelium-dependent dilators evoked greater vasodilation than combination of either dilator with SNP (ΔFVC from first dilator, ATP+ACh: 45±9 vs. SNP+ACh: 18±7 and ATP+SNP: 26±4 ml·min-1·100 mmHg-1, P<0.05). Phenylephrine was subsequently infused to evaluate α1‑adrenergic vasoconstriction. Phenylephrine elicited less vasoconstriction during infusion of ATP or ACh vs. SNP (ΔFVC, -25±3 and -29±4 vs. -48±3%; P<0.05). The vasoconstrictor response to phenylephrine was further diminished during combined infusion of ATP+ACh (-13±3%; P<0.05 vs. ATP or ACh alone) and was less than that observed when either dilator was combined with SNP (SNP+ACh: -26±3%; ATP+SNP: -31±4%; both P<0.05 vs. ATP+ACh). We conclude that endothelium-dependent agonists interact to elicit vasodilation and limit α1‑adrenergic vasoconstriction in humans.

PEROXIDE STIMULATION OF PGI3 AND DIHOMO-PGI2 IN ENDOTHELIUM

1987 ◽  
Author(s):  
J C Bordet ◽  
M Guichardant ◽  
M Lagarde
Keyword(s):  
Vascular Endothelium ◽  
Gas Chromatography Mass Spectrometry ◽  
Efficient Synthesis ◽  
Competitive Inhibitors ◽  
Silyl Derivatives ◽  
Adrenic Acid ◽  
High Peroxide ◽  
Prostacyclin Synthase ◽  
Docosatetraenoic Acid ◽  
Stimulation Of

Human umbilical endothelial cell (EC) monolayers incubated with eicosapentaenoic acid (EPA) produce small amounts of prostaglandin E3 (PGI3). We have previously shown that this metabolite is markedly enhanced in EC supernatant by co-incubating EPA with arachidonic acid (AA) (BBRC 135, 403, 1986). Moreover we found that PGF3a and PGE3 were similarly enhanced, and we concluded that such a stimulation occured at the cyclooxygenase rather than at the prostacyclin synthase level. It is generally assumed that cyclooxygenase is a peroxide-dependent enzyme and the present study shows that the potentiating effect of AA on EPA cyclooxygenation may be due to its hydroperoxy derivative, 15-HPETE. This has been established by measuring prostanoids of the trienoic series from (14-C)EPA and by detection of their metoxy-pentafluorobenzyl-trimethyl silyl derivatives from unlabelled EPA by gas chromatography-mass spectrometry. The potentiating effect of n-6 hydroperoxy derivative of linoleic acid (13-HPODE) was even higher than that of 15-HPETE. In addition, the cyclooxygenation of docosatetraenoic acid (DTA) or adrenic acid, was found to be also potentiated by 15-HPETE and 13-HPODE, but higher concentrations were required for the efficient synthesis of dihomo-PGI2. Concentrations of peroxides required for such potentiations were however far lower (−2μM) than those inhibiting prostacyclin synthase (≥100μM under our conditions). EPA and DTA, as competitive inhibitors of AA cyclooxygenation, appeared to need a higher peroxide tone than AA for their own metabolism. The biological relevance of DTA is not proved at this day, and dihomo-PGI2 has been found less active than PGI2. In contrast, PGI3 has been assumed to exhibit similar antiaggregatory effect than PGI2. EPA may then beneficially enhance the prostacyclin potential of vascular endothelium especially in conditions where a high peroxide tone is suspected like ageing or diabetes

Extracellular Nucleotides ATP and UTP Induce a Marked Acute Release of Tissue-type Plasminogen Activator In Vivo in Man

2001 ◽  
Vol 85 (05) ◽  
pp. 875-881 ◽  
Author(s):  
Thórdís Hrafnkelsdóttir ◽  
David Erlinge ◽  
Sverker Jern
Keyword(s):  
Vascular Endothelium ◽  
Adenosine Receptors ◽  
Healthy Subjects ◽  
Tissue Injury ◽  
Extracellular Nucleotides ◽  
Tissue Type ◽  
Type Plasminogen Activator ◽  
Ischemic Tissue ◽  
Stimulation Of

SummaryExtracellular nucleotides such as ATP and UTP are released by activation of platelets and ischemic tissue injury. The aim of the present study was to investigate whether ATP and UTP can induce acute tPA release from the vascular endothelium in vivo. Nine healthy subjects were studied in a perfused-forearm model during stepwise intraarterial infusions of ATP and UTP (10-200 nmol/min), and UTP during inhibition of prostanoid and NO synthesis by indomethacin and L-NMMA. ATP and UTP induced a similar and marked stimulation of forearm tPA release which increased 11- and 18-fold above baseline (p ≤ 0.01 for both) in conjunction with pronounced vasodilation. Neither the acute tPA release nor the vasodilation could be abrogated by NO and prostanoid synthesis inhibition. The similar effect of ATP and UTP suggests that P2Y rather than adenosine receptors mediate the response. Release of extracellular nucleotides in ischemic tissue may induce a pronounced activation of the endogenous fibrinolytic system.

Activation of endothelial cell phospholipase D by polycations

1997 ◽  
Vol 272 (4) ◽  
pp. L608-L613 ◽  
Author(s):  
S. Vepa ◽  
W. M. Scribner ◽  
V. Natarajan
Keyword(s):  
Phospholipase D ◽  
Vascular Endothelium ◽  
Cellular Response ◽  
Specific Protein ◽  
Cellular Functions ◽  
Kinase C ◽  
Naturally Occurring ◽  
Molecular Sizes ◽  
Stimulation Of ◽  
Specific Protein Kinase

Naturally occurring polycations and cationic proteins are implicated in vascular disorders. It is known that activated leukocytes and platelets release polycations, such as polylysine (PLys), of varying molecular sizes into the vasculature, and some of these have been described to be bactericidal. Polycations interact with endothelial cells (ECs) and cause alterations in permeability and cellular functions. The precise mechanism(s) by which polycations bring about cellular changes is unknown. Here, we report that the polycations PLys and polyarginine (PArg) induce phospholipase D (PLD) activation in ECs. Polycation-mediated PLD activation was both time and concentration dependent, and activation of PLD was not due to cytotoxicity. PArg was more potent compared with PLys of the same molecular weight in stimulation of PLD. Treatment with bisindolylmaleimide, a specific protein kinase C (PKC) inhibitor, and heparin attenuated polycation-mediated PLD activation. Furthermore, downregulation of PKC by 12-O-tetradecanoylphorbol-13-acetate (100 nM, 18 h) also blocked polycation-mediated PLD stimulation. These data suggest that polycation-mediated PLD stimulation probably involves PKC and may represent an important cellular response to leukocyte/platelet activation in the vascular endothelium.

Angiotensinergic stimulation of vascular endothelium in mice causes hypotension, bradycardia and attenuated angiotensin response

2008 ◽  
Vol 45 (4) ◽  
pp. S24
Author(s):  
Takanobu Takezako ◽  
Ramaswamy Ramchandran ◽  
Yasser Saad ◽  
Naoki Makino ◽  
Sadashiva S. Karnik
Keyword(s):  
Vascular Endothelium ◽  
Stimulation Of

Effects of 5-5'-Diphenyl-2-thiohydantoin (DPTH) and Thyroxine on the Ultrastructure and Chemical Composition of Rat Liver

1971 ◽  
Vol 29 ◽  
pp. 570-571
Author(s):  
E. A. Elfont ◽  
R. B. Tobin ◽  
D. G. Colton ◽  
M. A. Mehlman
Keyword(s):  
Chemical Composition ◽  
Rat Liver ◽  
Future Study ◽  
Mode Of Action ◽  
Liver Mitochondria ◽  
Rat Liver Mitochondria ◽  
Effective Inhibitor ◽  
Biochemical Effects ◽  
Glycerophosphate Dehydrogenase ◽  
Stimulation Of

Summary5,-5'-diphenyl-2-thiohydantoin (DPTH) is an effective inhibitor of thyroxine (T4) stimulation of α-glycerophosphate dehydrogenase in rat liver mitochondria. Because this finding indicated a possible tool for future study of the mode of action of thyroxine, the ultrastructural and biochemical effects of DPTH and/or thyroxine on rat liver mere investigated.Rats were fed either standard or DPTH (0.06%) diet for 30 days before T4 (250 ug/kg/day) was injected. Injection of T4 occurred daily for 10 days prior to sacrifice. After removal of the liver and kidneys, part of the tissue was frozen at -50°C for later biocheailcal analyses, while the rest was prefixed in buffered 3.5X glutaraldehyde (390 mOs) and post-fixed in buffered 1Z OsO4 (376 mOs). Tissues were embedded in Araldlte 502 and the sections examined in a Zeiss EM 9S.Hepatocytes from hyperthyroid rats (Fig. 2) demonstrated enlarged and more numerous mitochondria than those of controls (Fig. 1). Glycogen was almost totally absent from the cytoplasm of the T4-treated rats.

Gap junctions in the prothoracic glands of the tobacco hornworm, Manduca sexta

1992 ◽  
Vol 50 (1) ◽  
pp. 706-707
Author(s):  
Ji-da Dai ◽  
M. Joseph Costello ◽  
Lawrence I. Gilbert
Keyword(s):  
Gap Junctions ◽  
Small Molecules ◽  
Manduca Sexta ◽  
Freeze Fracture ◽  
Cell Communication ◽  
Cellular Level ◽  
Thin Sections ◽  
Prothoracic Glands ◽  
Polyhydroxylated Steroids ◽  
Stimulation Of

Insect molting and metamorphosis are elicited by a class of polyhydroxylated steroids, ecdysteroids, that originate in the prothoracic glands (PGs). Prothoracicotropic hormone stimulation of steroidogenesis by the PGs at the cellular level involves both calcium and cAMP. Cell-to-cell communication mediated by gap junctions may play a key role in regulating signal transduction by controlling the transmission of small molecules and ions between adjacent cells. This is the first report of gap junctions in the PGs, the evidence obtained by means of SEM, thin sections and freeze-fracture replicas.

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